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by **admin_pornrev** » Sun Jul 12, 2009 5:43 pm

Extract from www.motherjones.com

Estrogen Kills Fish
— By Julia Whitty | Thu June 4, 2009 4:48 PM PST

Estrogen is bad for fish. In more ways than we thought.

We know that estrogen and estrogen-mimicking chemicals known as endocrine disruptors cause intersex fish—that is, males with immature female egg cells in their testes.

New research finds that fish exposed to estrogen produce less immune-related proteins, making them more susceptible to disease. This suggests why fish in the Shenandoah and Potomac Rivers are simultaneously afflicted by mass kills, lesions, and intersex fish.

US Geological Survey researchers suspected that estrogens were causing fish kills and fish lesions as well as intersex fish in the two river systems. So they exposed largemouth bass to estrogen and found the fish produced less hepcidin—an iron-regulating hormone of mammals, fish, and amphibians.

Exactly what hepcidin does to boost immune systems is unclear. But it may act as an antimicrobial peptide, the first line of defense against disease-causing bacteria, fungi, and viruses. Or it might affect the iron balance in infected vertebrates. Or both.

We do know we're loosing megatons of synthetic chemicals into waterways every year. Most are plastics additives, surfactants, birth control agents, antimicrobials, pharmaceuticals, personal care products, or controls for insect, weed, and fungal populations.

But all too many wind their way from industry, livestock, irrigation, sewage, and storm run-off into lakes, ponds, oceans, marshes, streams, rivers, and groundwater—eventually into fish.

And from there into humans, perhaps accounting for the alarming rise of human male reproductive disorders in recent years, including birth defects of the penis, undescended testes, reduced sperm production, and testicular cancer.

You think that might slow down the chemical pipeline. Especially in rivers so close to Washington, DC. But apparently money is worth more than masculinity.

MORE INFO ON HOW ESTROGEN IS KILLING THE WORLD COMMING SOON

by **admin_pornrev** » Mon Jul 13, 2009 2:01 pm

Extract from www.motherjones.com

1. Environmental estrogens: A hazard to human reproductive health?
Written by Dr Nigel Brooks

Dr Nigel Brooks, Zeneca CTL
Download the briefing as a PDF file

During our everyday life we are continuously exposed to a cocktail of chemicals which can mimic the actions of the female hormone, estrogen. There is concern that these chemicals, known as environmental estrogens, may have adverse effects on reproductive health in humans and wildlife. Researchers have a key role to play in understanding how these chemicals control the reproductive system, so that we are better able to judge if they really are a hazard to human reproductive health.
The perceived threat - scare or reality?

Declining sperm counts in men, an increased incidence in breast cancer, feminised fish, alligators with small phalluses; these are just some of the adverse changes in reproductive health, reported to have taken place in the past few years, and with one thing in common; they can all be caused by the female hormone estrogen. Recent research has shown that many man made chemicals can act as weak estrogens, mimicking in part the actions of our own natural hormones. These chemicals are present throughout our daily life. They can be found in the plastic lining of food cans, in pesticides, in plastics and in paints. The question is - are these chemicals actually responsible for the increased level of adverse reproductive effects? Is this a scare or reality? Tissue differences in the type and amount of estrogen receptor may explain how natural, synthetic and environmental estrogens could have specific effects in the body. ERa which predominates in Cell 1, prefers to bind a particular type of estrogen (estrogen A) whereas ERb located in Cell 2 (see figure below), prefers another (estrogen B). Following interaction with these estrogens the receptors pair up and bind to estrogen response elements (ERE) in target genes. These genes may contain ERE's which also have a preference for each of the receptors. These complex control mechanisms would allow different types of estrogen (perhaps environmental estrogenic chemicals) to act in a particular part of the body to change the activity of a specific target gene.
The uncertainty

Researchers have known for some time now that if the body is exposed to excessive amounts of estrogen at certain stages in development, this can have adverse reproductive effects. For example, females exposed to estrogens during critical periods of brain sexual development are unable to ovulate as adults, and exhibit male patterns of sexual behaviour. Could environmental estrogens mimic these adverse effects? Another example is found in an intriguing hypothesis to explain how human sperm counts may have declined in the past 50 years. A man's capacity to produce sperm is determined by the number of specialised cells in the testis, called Sertoli cells. Sertoli cell number is regulated by follicle stimulating hormone (FSH) which is secreted from the pituitary gland, but FSH can only do this during a critical period in fetal and early neonatal life. If animals are exposed to a synthetic estrogen called diethylstilbestrol during this critical period, this reduces the amount of FSH produced in the fetal pituitary gland and the testes in the male offspring are smaller, with fewer Sertoli cells.

Testes in the male offspring are smaller, with fewer Sertoli cells.

These animals produce less sperm when they reach adulthood. Can environmental estrogens have similar effects? Researchers have recently shown that when pregnant animals are exposed to a chemical called octylphenol, the secretion of FSH in the fetus is reduced. Octylphenol is a break-down product of a group of chemicals which are used in the manufacture of some detergents and paints, If exposure to this chemical were to take place for long enough during the sensitive period, then this may lead to smaller testes and reduced sperm counts. But a word of caution. We are still uncertain as to the extent to which the human body is actually exposed to chemicals such as octylphenol, and as yet there is no direct proof that there is any link between chemical exposure and changes in sperm counts in man.

Estrogen receptors are promiscuous. They allow many hundreds of different chemicals to bind to them.
Unravelling the mystery - the role of research

In order for estrogenic hormones to exert their many effects in the body of humans, they must first bind to an estrogen receptor, a specialised protein located in target cells, which recognises the hormone and allows it to regulate specific estrogen responsive genes within the cell. Estrogen receptors are promiscuous. They allow many hundreds of different chemicals to bind to them. In some cases the chemicals have structures which are so dissimilar to that of the natural hormone, estradiol, that they would never normally be thought of as having hormonal activity. These chemicals are very weak estrogens by comparison with naturally occurring hormones, but if given in high enough amounts they can activate estrogen receptors in much the same way as natural hormones do. Until recently, it was thought that there was only one estrogen receptor. However, researchers have now discovered a second estrogen receptor (ERb) which prefers to bind certain environmental and natural estrogens compared with the original estrogen receptor (ERa). This new receptor is located in higher amounts in specific tissues in the body, such as the prostate, ovary and brain. Scientists now believe that this combination of different types of estrogen receptor and differing tissue distribution, may be crucial in determining if a particular part of the body is likely to be affected by natural or environmental estrogens (see figure).
Where to from now?

The topic of environmental estrogens is of growing interest. Government agencies in the US and in Europe are eager to introduce methods for testing and interpreting data to allow an assessment of the threat to human health from exposure to endocrine disruptors. Even with a variety of different tests in place, human hazard assessment will be a challenging task. Researchers have an exciting time ahead, as they unravel the many complex ways in which natural and environmental estrogens interact with the reproductive organs.

by **admin_pornrev** » Mon Jul 13, 2009 2:29 pm

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Feminizing The World
Extract from www.motherjones.com

By Dr. Randy W. - 2006-04-21
Find more articles like this in our Disability Sexuality category.

While science is busy scurrying around trying to find the genes that cause homosexuality, a new chemotherapeutic agent to cure female cancers, new diagnostic tests to detect prostate cancer earlier, throwing more and more money at research, the answer likely lies right under our noses.

Sex hormones are critical in governing a broad range of biological activities, including the development of the sexes. Early in fetal life, through a series of molecular switches, hormones signal the development of either male or female structures. It is the relative amount of female-to-male hormones that dictates whether we become male or female.

Over the past couple of decades, research has demonstrated that a kaleidoscope of synthetic chemicals and pollutants that have been introduced into our environment are capable of mimicking the effects of these natural sex hormones.

There are now some 45 environmental pollutants known to cause changes in the reproductive system. Examples include herbicides, pesticides, fungicides, insecticides, nematocides, PCB's, styrene, combustion pollutants, a variety of metals, ingredients in plastics, break-down products of common detergents and other industrial by-products and commercial chemicals.

Estrogenic pesticides have now even appeared at detectable levels in the Antarctic penguin. 2, 4-D is the largest selling broad-leaf herbicide in North America, with some 60 million pounds of it and its chemical analogs used annually in the United States. This compound is another estrogen mimicker. A diverse array of chemicals, many structurally quite unlike natural hormones, specifically mimic the female sex hormone, estrogen. Thus, it is not possible to determine by molecular analysis whether chemicals will mimic sex hormones until they are released into our environment and produce damage.

Environmental hormone mimickers may not only induce female and male cancers - but in levels far less than required to produce cancer - may trigger reproductive effects.

Here are examples of what these pollutants are doing in the biological world: The eggshells of many birds are thinning. The result is that embryonic birds can be crushed by the mother, as has occurred in the past as a result of DDT contamination.

Gulls have developed grossly feminized reproductive tracts and some female gulls, called lesbian gulls, share nests. Gonads developed intersex characteristics - such that tissues had both the characteristics of ovaries and testicles. Males lost interest in mating and developed feminized sex organs. Reproduction in bald eagles is known to drop when PCB's in their bodies exceed 4 to 6 parts per million, or when DDE, a descendant of DDT exceeds 1 part per million. In the Great Lakes area, eggs are being found with PCB concentrations as high as 120 parts per million.

In Florida, there are super female alligators with ratios of estrogen to testosterone twice as high as normal. Some entire groups of hatchlings show no characteristics of maleness at all. Males had what looked like ovaries and stunted genitalia, and the ovaries of the females, on the histological (tissue) level, looked as though they were exhausted. These anomalies found in animals at Lake Apopka were traced to an effluent from the Tower Chemical Company. Their pesticide, Dicofol, is a molecule that looks identical to DDT except it has an extra oxygen atom. Spills into the lake were also laced with DDT and DDE, even though these chemicals have been outlawed long ago. Remember, although the U.S. may ban domestic sale of some chemicals, that does not prevent manufacturers from producing them for export. (Not an admirable ethic, to be sure.)

Trout exposed to industrial effluent have 500 to 100,000 fold increases in vitel-logenin, a biomarker for exposure to estrogenic pollutants.

The Pallid Sturgeon, an endangered fish native to the Mississippi and Missouri rivers, simply doesn't reproduce anymore. Some have gonads neither distinctly male nor female.

Ethynylestradiol is the main estrogenic compound in birth control pills. Women who take the pill excrete the compound in their urine, which then passes through water treatment plants and on into the environment. The level of such birth control pill by-products in potable water supplies is in concentrations below the limits of detection. Nevertheless, these compounds are exerting biological effects on wildlife in the waterways.

Breakdown products of alkyl phenol polyethoxylates, a class of surfactants used in various soaps and even in pesticides, herbicides and cosmetics, have the ability to directly activate the body's estrogen receptors. These compounds bioaccumulate in tissues, particularly fat tissues. Some 360 million pounds of these surfactants are sold in the United States each year.

Even electromagnetic fields (EMF) generated by power lines, household appliances and wiring demasculinize mature males. EMF abnormalities in rats include the development of abnormal testes and prostate glands. Researchers remark that the reproductive system of the rat is "built like a Sherman tank." Certainly, then, if they are affected by electromagnetic fields, humans may be even more susceptible.

Sixty-seven percent of male Florida panthers, an endangered species with only about 30 to 50 animals still surviving, have undescended testicles. Only 14% of males had this condition just 10 years earlier. Even normal males are producing abnormal and deformed sperm cells. Some males had an estrogen to testosterone ratio that was inverted, having more estrogen than testosterone rather than vice-versa.

Environmental estrogenic pollutants are particularly dangerous to the male since the male's reproductive system is more sensitive to the effects of estrogen than any other organ system.

Even though adult animals may appear perfectly normal, they may be reproductively dysfunctional. Some species of animals, though apparently healthy right now, may be in effect extinct.

The ubiquitous nature of feminizing hormones in our environment effectively bathes us in a sea of estrogenic substances. The full consequences of this exposure are only beginning to be understood. We are breathing it in our air, eating it on our fruit, and absorbing it through our skin; children are receiving it in the blood and milk from their mothers.

Many countries are now seeing a sharp rise in testicular cancer, more than tripling over the past 50 years. Also, the sperm count in men has fallen almost 50%, as documented in a study of some 15,000 men between the years of 1940 and 1990.

The rate of cryptorchidism (undescended testicles) has increased by almost two-fold in the years from 1950 to 1970. [We are so clever. First we saturate the bodies of our babies with feminizing pollutants and cause their testicles not to descend, and then we cleverly implant a silicone prosthetic testicle in the scrotum so that they appear normal. Then, the silicone causes an autoimmune disturbance resulting in the debilitating disease lupus erythematosus. (Vol. 8, No. 2).]

Another condition, hypospadias, in which the urinary tract is not formed properly in the fetus, doubled between the years 1964 and 1982.

Early exposure to feminizing hormone pollutants may disrupt the Sertoli cell in the testicles. These cells direct the development and descent of the testes and control the development of sperm and the secretion of male hormones responsible for masculinization. Sertoli cells are particularly sensitive to follicle stimulating hormone (FSH), but exogenous estrogenic pollutants inhibit FSH. Reproductive problems experienced in the general population are identical to the problems experienced by the male offspring of women who, during pregnancy, receive treatment with diethylstilbestrol (DES), a potent synthetic estrogen. The broad range of estrogenic substances in our environment makes it almost impossible to determine a person's exposure. Though a limit might be set on each of the estrogenic compounds, their effects are additive. Thus, if a person were only taking a tenth of the supposedly safe dosage of 10 different compounds, the additive effect would be toxic. In our clamor to rid our environment of carcinogenic (cancer-causing) substances, we have ignored the estrogenic effects. Alarmingly, the threshold levels for compounds to produce reproductive and sexual aberrations are often far less than those necessary to produce cancer.

If estrogenic compounds are capable of changing virtually every reproductive tissue in the body, as well as disrupting hormone balances, might they not also affect sexual behavior? Might the rise in sexual crimes and homosexuality be at least partially a result of our swimming in an increasingly concentrated sea of estrogens?

What can we do? First of all, take seriously the dangers of synthetic chemicals and pollutants in our food and environment. Don't minimize the dangers or worry about being picayunish. It is likely that you simply can't be careful enough. Also, do your part to decrease industrialization by decreasing consumption and waste. By decreasing demand we decrease the odds of pollution.

It is of interest that phytoestrogens found in whole grains such as rye, as well as in legumes such as soy - although estrogenic - possibly have the ability to compete against environmental pollutant estrogens. They are antagonistic to estrogenic adverse effects and apparently do not exert the harmful estrogenic effects of the environmental pollutants.

Since estrogenic compounds are fat soluble, the more fat you have, the greater the potential reservoir for these pollutants. This is yet another reason to maintain healthy body weight.

The ubiquitous nature of synthetic estrogenic compounds and their potential adverse effects is a serious and insidious threat to life on Earth. The power to change things is in our hands.

We must restore our natural context if we are to enjoy health and leave a livable world to our children.

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